Ask about this productRelated genes to: PDIK1L Blocking Peptide
- Gene:
- PDIK1L NIH gene
- Name:
- PDLIM1 interacting kinase 1 like
- Previous symbol:
- -
- Synonyms:
- CLIK1L
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-26
- Date modifiied:
- 2016-10-05
Related products to: PDIK1L Blocking Peptide
Related articles to: PDIK1L Blocking Peptide
- Prostate cancer demonstrates significant metabolic heterogeneity, but its role in therapeutic resistance and disease progression remains unclear. This study investigates the clinical implications of metabolic diversity and identifies potential biomarkers for precision oncology. - Source: PubMed
Publication date: 2025/11/04
Wang ZhongyuanGe QintaoAihetaimujiang AnwaierZhang JiLu JiaheYang JianfengChen YonghaoQin BinZhang HailiangXu Wen-HaoYe Dingwei - Oocyte aging is a significant factor in the negative reproductive outcomes of older women. However, the pathogenesis of oocyte aging remains unclear. This study aimed to identify the hub genes involved in oocyte aging via bioinformatics methods. - Source: PubMed
Publication date: 2024/11/14
Luo XiLiang MingmingZhang DandanHuang Ben - The correlation between hypoxia and tumor development is widely acknowledged. Meanwhile, the foremost organelle affected by hypoxia is mitochondria. This study aims to determine whether they possess prognostic characteristics in lung adenocarcinoma (LUAD). For this purpose, a bioinformatics analysis was conducted to assess hypoxia and mitochondrial scores related genes, resulting in the successful establishment of a prognostic model. Using the single sample Gene Set Enrichment Analysis algorithm, the hypoxia and mitochondrial scores were computed. Differential expression analysis and weighted correlation network analysis were employed to identify genes associated with hypoxia and mitochondrial scores. Prognosis-related genes were obtained through univariate Cox regression, followed by the establishment of a prognostic model using least absolute shrinkage and selection operator Cox regression. Two independent validation datasets were utilized to verify the accuracy of the prognostic model using receiver operating characteristic and calibration curves. Additionally, a nomogram was employed to illustrate the clinical significance of this study. 318 differentially expressed genes associated with hypoxia and mitochondrial scores were identified for the construction of a prognostic model. The prognostic model based on 16 genes, including PKM, S100A16, RRAS, TUBA4A, PKP3, KCTD12, LPGAT1, ITPRID2, MZT2A, LIFR, PTPRM, LATS2, PDIK1L, GORAB, PCDH7, and CPED1, demonstrates good predictive accuracy for LUAD prognosis. Furthermore, tumor microenvironments analysis and drug sensitivity analysis indicate an association between risk scores and certain immune cells, and a higher risk scores suggesting improved chemotherapy efficacy. The research established a prognostic model consisting of 16 genes, and a nomogram was developed to accurately predict the prognosis of LUAD patients. These findings may contribute to guiding clinical decision-making and treatment selection for patients with LUAD, ultimately leading to improved treatment outcomes. - Source: PubMed
Publication date: 2024/06/17
Zhao WenhaoHuang HuaZhao ZexiaDing ChenJia ChaoyiWang YingjieWang GuannanLi YongwenLiu HongyuChen Jun - Acute myeloid leukemia (AML) cells rely on phospho-signaling pathways to gain unlimited proliferation potential. Here, we use domain-focused CRISPR screening and identify the nuclear phosphatase SCP4 as a dependency in AML, yet this enzyme is dispensable in normal hematopoietic progenitor cells. Using CRISPR exon scanning and gene complementation assays, we show that the catalytic function of SCP4 is essential in AML. Through mass spectrometry analysis of affinity-purified complexes, we identify the kinase paralogs STK35 and PDIK1L as binding partners and substrates of the SCP4 phosphatase domain. We show that STK35 and PDIK1L function catalytically and redundantly in the same pathway as SCP4 to maintain AML proliferation and to support amino acid biosynthesis and transport. We provide evidence that SCP4 regulates STK35/PDIK1L through two distinct mechanisms: catalytic removal of inhibitory phosphorylation and by promoting kinase stability. Our findings reveal a phosphatase-kinase signaling complex that supports the pathogenesis of AML. - Source: PubMed
Polyanskaya Sofya AMoreno Rosamaria YLu BinFeng RuopengYao YuIrani SeemaKlingbeil OlafYang ZhaolinWei YiliangDemerdash Osama EBenjamin Lukas AWeiss Mitchell JZhang Yan JessieVakoc Christopher R - This review aims to assess the current and past literature for efficacious non-invasive diagnostic markers for earlier detection of endometriosis. We briefly discussed the associations of endometriosis with other autoimmune diseases (AID), as well as the broad changes that occur within the immune system. Specifically, we focused on the usage of various autoantibodies as a potential non-invasive diagnostic tool. Autoantibodies have been noted in the literature since the 1980s and their usage could possibly reduce the delay of an endometriosis diagnosis. Our search concluded that various anti endometrial antibodies may offer useful diagnostic tools. Anti-SLP2, anti-TMOD3, anti-TPM3, and anti-PDIK1L are particularly useful for early diagnosis in minimal to mild endometriosis. Anti-alpha enolase could also be used but yields results similar to CA125. Other non anti endometrial antibodies like anti-IMP1, anti-CA, aCL, anti-STX5 may be used as additional non-invasive diagnostic tools. Anti-TPO may be beneficial in patients in endometriosis patients with concurrent polycystic ovaries syndrome (PCOS). As the pathogenesis of endometriosis continues to reveal itself, more autoantibodies are being discovered and they may offer useful non-invasive tools for the early diagnosis of endometriosis. - Source: PubMed
Publication date: 2021/03/13
Greenbaum HilaGalper Bat-El LugassyDecter Dean HEisenberg Vered H